In the same in vitro cultures in which human lymphocytes proliferate in response to mitogens or specific antigens, the antiviral protein, interferon, is produced as a mediator of cellular immunity. Early in culture, the interferon is a product only of T (thymic derived) lymphocytes, but later on, of B (bone marrow derived) lymphocytes as well, but in each instance the presence of macrophages serves to augment the production of interferon by lymphocytes. In the proposed research program we shall determine if all, or just a subset, of human T or B lymphocytes can produce interferon, and if agents which alter the surface components of macrophages (glutaraldehyde, trypsin, neuraminidase, anti-macrophage serum) will affect their ability to augment lymphocyte interferon production. In addition, we shall study the affect on lymphocyte interferon production of agents which alter intracellular levels of cyclic AMP (Prostaglandin E1, dibutyrl cyclic AMP, theophylline, cholera toxin) and agents which affect microfilament (cytochalasin B) or microtubular function (colchicine, vinblastine). We shall determine if mitogen stimulated interferon has any properties in addition to its antiviral effect (i.e., in regulation of lymphocyte proliferation or macrophage homeostasis). Finally, we shall quantitate the amount of interferon produced by highly purified preparations of T lymphocytes from patients with various disease states (selective IgA deficiency, thymic insufficiency, Wiskott Aldrich Syndrome, ataxia telangiectasia, subacute sclerosing panencephalitis) to assess the competence of their T lymphocyte effector function.